Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A platelet indirect radio-active Coombs test has been described. The technique for purification and labelling the antiglobulin has been precised. This test allows the typing of platelets in the PLA system and the study of sera from mothers of thrombocytopenic child. As examples, four families of neonatal thrombocytopenia are reported, with PLA1 negative mother. In the serum of three of these mothers, we could demonstrate anti-PLA antibodies in spite of a negative platelet complement fixation. This test has many advantages compared to other tests such as platelet complement fixation, assay for blocking antibodies or antiglobulin consumption: it gives objective and quantitative results and is highly reproducible, anticomplementary serum may be tested. It has enabled us to select PLA1 negative donors for exsanguino-transfusions of thrombocytopenic children born from PLA1 negative mothers.
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PMID:[Typing and detection of antibodies in the PLA system (platelet). Application to the study of neonatal thrombopenia by feto-maternal PLA allo-immunisation]. 100 52

Desmopressin (DDAVP) 0.3 micrograms/kg was administered intravenously to three normal volunteers and 12 patients with von Willebrand's disease (vWD), congenital or acquired platelet function defect, or uremic bleeding to assess its effects and side effects. DDAVP significantly shortened the bleeding time as compared with basal values. The mean peak post-DDAVP level of factor VIII coagulant activity increased 5.9 +/- 0.5 (mean +/- SEM) fold, von Willebrand factor antigen increased 3.7 +/- 0.3 fold, von Willebrand factor ristocetin cofactor activity increased 4.6 +/- 0.6 fold and the tissue-type plasminogen activator antigen increased 3.4 +/- 0.6 fold. Analysis of the multimeric structure of the von Willebrand factor revealed that type I vWD had complete correction after DDAVP infusion transiently. Except for a mild drop in both systolic and diastolic blood pressures, few side effects were noted. By concomitant intravenous infusion of DDAVP and oral administration of tranexamic acid, we successfully treated two cases of type I vWD undergoing tooth extraction, and one case of acquired bleeding disorder undergoing a biopsy of a mandibular mass, and a uremic patient complicated by intractable traumatic hematuria. Our experiences confirmed that most patients with vWD and some patients with congenital or acquired bleeding disorders can be treated effectively by DDAVP infusion without the need for plasma product replacement. In this study we found that a patient with a variant form of type I vWD had prolongation of the bleeding time, thrombocytopenia and platelet aggregation after DDAVP infusion.
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PMID:Experience of desmopressin (DDAVP) administration in patients with congenital and acquired bleeding disorders. 136 75

A monoclonal antibody, LK-4, has been developed which distinguishes platelet PLA1/PLA1, PLA1/PLA2 and PLA2/PLA2 genotypes on platelet glycoprotein GPIIIa of Triton-solubilized platelet extracts. An ELISA assay has been developed which traps GPIIIa with Concanavalin A, enriching the platelet extract for the PLA antigens. A second monoclonal antibody, DEK-10, which reacts equally with GPIIIa of PLA1/PLA1 and PLA2/PLA2 platelet extracts is employed as an internal standard to correct for individual differences in GPIIIa content, GPIIIa extracted by Triton X-100 and GPIIIa trapped with Concanavalin A. This ELISA assay clearly differentiated 11 different PLA1/PLA1 subjects from eight PLA2/PLA2 women with a history of neonatal alloimmune thrombocytopenia as well as six unrelated obligate heterozygotes and should be useful in evaluating the PLA genotype of pregnant women and their families.
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PMID:Development of a monoclonal antibody capable of differentiating platelet PLA1/PLA1, PLA1/PLA2 and PLA2/PLA2 genotypes. 152 Jun 9

Endotoxin plays an important role in the pathogenesis of septicaemia by activation of cellular and plasmatic systems. This study was performed to investigate the effects of infusion of endotoxin in rabbits by measuring the activation of cellular and plasma systems. Endotoxin was infused at a rate of 1 mg/kg body wt for 10 min, which caused death of all rabbits within 72 h. Endotoxin induced early leukopenia and thrombopenia, increased plasma levels of beta-glucuronidase and leukotriene B4 (LTB4), and decreased complement total hemolytic activity (CH50) and tissue plasminogen activator (t-PA) activity. These observations correlate with the cellular and plasma changes that have been documented in severely ill endotoxemic patients. Therefore, we conclude that this endotoxin model in rabbits is a valuable tool for investigation of pathophysiology and treatment of endotoxic shock.
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PMID:Activation of plasma systems and blood cells by endotoxin in rabbits. 164 34

Endotoxemia in patients can lead to sepsis and shock by activation of cellular and plasmatic systems. Corticosteroids are described to have a beneficial effect on these phenomena. In this study of controlled endotoxic shock, we investigated the protective effects of prophylactic corticosteroid treatment against activation of cellular and plasmatic systems. In this respect, a low-dose methylprednisolone (1 mg/kg body wt) treatment was compared with that of a high-dose methylprednisolone (40 mg/kg body wt) treatment. Endotoxin infusion induced death of all rabbits, which was associated with leukopenia, thrombopenia, increased levels of beta-glucuronidase, and leukotriene B4 (LTB4) and decreased levels of complement total hemolytic activity (CH50) and tissue plasminogen activator (t-PA) activity. Both methylprednisolone regimens prevented death of the rabbits after endotoxin infusion, which correlated with a significant decrease of the granulocyte release product beta-glucuronidase (P less than 0.01). The early leukopenia and thrombopenia were not prevented; however, both cell numbers returned more rapidly to baseline values than in the placebo group (P less than 0.01, P less than 0.05). The LTB4 and CH50 concentration and t-PA activity did not differ significantly between the treated and placebo groups. These results indicate that although methylprednisolone has no inhibitory effect on the activation of the complement, arachidonic acid, and fibrinolytic systems, it protected the animals from the deleterious effects of endotoxin shock by inhibition of leukocyte activation. In this regard a low dosage of methylprednisolone is equally effective as the most often recommended high dose.
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PMID:Methylprednisolone prophylaxis protects against endotoxin-induced death in rabbits. 164 35

The HPA-1 platelet antigenic system (PLA/Zw) is involved in most cases of antiplatelet alloimmunization. The two alleles HPA-1a and HPA-1b are likely to differ only at the amino acid position 33. This difference is probably due to a unique mutation at base pair position 196 on the glycoprotein IIIa gene which encoded this antigen. Anti HPA-1a alloimmunization is responsible for neonatal thrombocytopenia and post-transfusion purpura. Most immunized women belong to the HLA DR3, DRw52a phenotype, suggesting that this class II molecule may play a role in the presentation of HPA-1a peptide to specific helper T cells.
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PMID:[Anti PLA or anti HPA-1 platelet allo-immunization]. 183 35

Thirty-four patients envenomed by Bothrops jararaca in Brazil were studied. Of these, 20 (59%) had incoagulable blood associated with local and/or systemic bleeding and 10 of the 20 were thrombocytopenic. Among 14 patients with coagulable blood, 6 (43%) had bleeding symptoms and 3 (21%) were thrombocytopenic. High levels of von Willebrand factor (vWF), plasminogen activator inhibitor type 1 (PAI-1) and tissue type plasminogen activator (t-PA) antigens were also recorded in some patients with systemic bleeding with or without incoagulable blood. These substances may have been released from endothelial cells. Admission serum venom antigen levels were similar in both groups. The study indicated that systemic haemorrhage may occur in patients with coagulable blood and thrombocytopenia and that coagulopathy is not therefore the primary cause of haemorrhage.
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PMID:Coagulopathy and haemorrhage in human victims of Bothrops jararaca envenoming in Brazil. 194 67

Allo-immune neonatal thrombopenia is to platelets what rhesus hemolytic disease is to red blood cells. There is a risk of haemorrhage when fetal platelets decreases below 50,000 per mm3. Such haemorrhage may occur at any time during the thrombopenia period. However they are mostly due to obstetrical traumatisms during delivery. Lethal complications and severe neurologic sequellae is estimated to affect about 30% of newborns: 1/3 these complications occur in utero and 2/3 during delivery. The authors have studied 3 familial cases of foeto-maternal allo-immunisation occurring with the PLA 1 system. They have made a briefing of the physiological, the pathological and the epidemiological aspects of such immunisation before insisting upon case findings of such affected fetus. A capillary blood sample taken from the scalp of the fetus at the beginning of labour allows a safe natural delivery if fetal blood count shows more than 50,000 platelets per mm3. A fetal blood sampling under ultrasonographic guidance will bring about to an early diagnosis and prognosis, this allowing an adequate treatment for fetus with a high risk of thrombopenia.
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PMID:[Neonatal alloimmune thrombocytopenia following immunization against the platelet antigen ZWA (PLA/1). 3 case reports in the same family and analysis of the literature]. 208 61

Fulminant hepatic failure causes a bleeding diathesis as a result of impaired synthesis of hepatic clotting factors, thrombocytopenia, fibrinolysis and disseminated intravascular coagulation. Administration of clotting factor concentrates can cause thrombosis in patients with acute hepatic failure. Regional infusion of recombinant tissue-type plasminogen activator may be used to induce local thrombolysis. A case report of a five-year-old child is presented and the literature is reviewed.
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PMID:Prothrombinex-induced thrombosis and its management with regional plasminogen activator in hepatic failure. 212 92

Plasma fibrinolytic factors were measured in 14 patients with chronic idiopathic thrombocytopenic purpura (ITP), in 5 patients with chronic central thrombocytopenia and in 16 healthy volunteers. The von Willebrand factor (vWF), tissue-type plasminogen activator (t-PA) and D-dimer (DD) antigens were found to be significantly higher in both patient groups than in the control group. No difference appeared in euglobulin fibrinolytic activity and plasminogen activator inhibitor activity. The increases in both t-PA and vWF suggest the occurrence of an endothelial cell stimulation, associated with the reduction of circulating platelet number. The correlation of increased DD and t-PA levels during ITP can be the proof of a fibrinolysis activation and suggest an antifibrinolytic role of platelets at physiological concentrations. These results can justify antifibrinolytic therapy in bleeding thrombocytopenic patients.
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PMID:Increased plasma tissue-type plasminogen activator levels in patients with chronic thrombocytopenia. 212 64


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